S. Giampaoli (Simona)http://repub.eur.nl/ppl/15400/
List of Publicationsenhttp://repub.eur.nl/eur_signature.pnghttp://repub.eur.nl/
RePub, Erasmus University RepositoryGlycated hemoglobin measurement and prediction of cardiovascular diseasehttp://repub.eur.nl/pub/58258/
Wed, 01 Jan 2014 00:00:01 GMT<div>E. di Angelantonio</div><div>P. Gao</div><div>H. Khan</div><div>A.S. Butterworth</div><div>D. Wormser</div><div>S. Kaptoge</div><div>S.R. Kondapally Seshasai</div><div>A. Thompson</div><div>S. Sarwar</div><div>J. Willeit</div><div>P.M. Ridker</div><div>E.L.M. Barr</div><div>K-T. Khaw</div><div>B.M. Psaty</div><div>H. Brenner</div><div>B. Balkau</div><div>J.M. Dekker</div><div>D.A. Lawlor</div><div>M. Daimon</div><div>J. Willeit</div><div>I. Njølstad</div><div>A. Nissinen</div><div>E. Brunner</div><div>L.H. Kuller</div><div>J.F. Price</div><div>J. Sundstrom</div><div>M.W. Knuiman</div><div>E.J.M. Feskens</div><div>W.M.M. Verschuren</div><div>A. Wald</div><div>S.J.L. Bakker</div><div>P. Whincup</div><div>I. Ford</div><div>U. Goldbourt</div><div>A. Gómez-de-la-Cámara</div><div>J. Gallacher</div><div>L.A. Simons</div><div>A. Rosengren</div><div>S.E. Sutherland</div><div>C. Björkelund</div><div>D.G. Blazer</div><div>S. Wassertheil-Smoller</div><div>A. Onat</div><div>A. Marín Ibañez</div><div>E. Casiglia</div><div>J.W. Jukema</div><div>L.M. Simpson</div><div>S. Giampaoli</div><div>B.G. Nordestgaard</div><div>R. Selmer</div><div>P. Wennberg</div><div>J. Kauhanen</div><div>J.T. Salonen</div><div>R. Dankner</div><div>E. Barrett-Connor</div><div>M. Kavousi</div><div>V. Gudnason</div><div>D.A. Evans</div><div>R.B. Wallace</div><div>M. Cushman</div><div>R.B. D'Agostino</div><div>J.G. Umans</div><div>Y. Kiyohara</div><div>H. Nakagawa</div><div>S. Sato</div><div>R.F. Gillum</div><div>A.R. Folsom</div><div>Y.T. Schouw</div><div>K.G.M. Moons</div><div>S. Griffin</div><div>N. Sattar</div><div>N.J. Wareham</div><div>E. Selvin</div><div>S.G. Thompson</div><div>J. Danesh</div>
C-reactive protein, fibrinogen, and cardiovascular disease predictionhttp://repub.eur.nl/pub/62285/
Thu, 04 Oct 2012 00:00:01 GMT<div>S. Kaptoge</div><div>E. di Angelantonio</div><div>L. Pennells</div><div>A.M. Wood</div><div>I.R. White</div><div>P. Gao</div><div>M. Walker</div><div>A. Thompson</div><div>S. Sarwar</div><div>M. Caslake</div><div>A.S. Butterworth</div><div>P. Amouyel</div><div>G. Assmann</div><div>S.J.L. Bakker</div><div>E.L.M. Barr</div><div>E. Barrett-Connor</div><div>E.J. Benjamin</div><div>C. Björkelund</div><div>H. Brenner</div><div>E. Brunner</div><div>R. Clarke</div><div>J.A. Cooper</div><div>P. Cremer</div><div>M. Cushman</div><div>G.R. Dagenais</div><div>R.B. D'Agostino</div><div>R. Dankner</div><div>G. Davey-Smith</div><div>D.J.H. Deeg</div><div>J.M. Dekker</div><div>G. Engström</div><div>A.R. Folsom</div><div>F.G.R. Fowkes</div><div>J. Gallacher</div><div>J.M. Gaziano</div><div>S. Giampaoli</div><div>R.F. Gillum</div><div>A. Hofman</div><div>B.V. Howard</div><div>E. Ingelsson</div><div>H. Iso</div><div>T. Jorgensen</div><div>S. Kiechl</div><div>A. Kitamura</div><div>Y. Kiyohara</div><div>W. Koenig</div><div>D. Kromhout</div><div>L.H. Kuller</div><div>D.A. Lawlor</div><div>T. Meade</div><div>A. Nissinen</div><div>B.G. Nordestgaard</div><div>A. Onat</div><div>D.B. Panagiotakos</div><div>B.M. Psaty</div><div>B. Rodriguez</div><div>A. Rosengren</div><div>V. Salomaa</div><div>J. Kauhanen</div><div>J.T. Salonen</div><div>J.A. Shaffer</div><div>S. Shea</div><div>I. Ford</div><div>C.D. Stehouwer</div><div>T.E. Strandberg</div><div>A. Tipping</div><div>A. Tosetto</div><div>S. Wassertheil-Smoller</div><div>P. Wennberg</div><div>R.G.J. Westendorp</div><div>P. Whincup</div><div>L. Wilhelmsen</div><div>M. Woodward</div><div>G.D.O. Lowe</div><div>N.J. Wareham</div><div>K-T. Khaw</div><div>N. Sattar</div><div>C. Packard</div><div>V. Gudnason</div><div>P.M. Ridker</div><div>M.B. Pepys</div><div>S.G. Thompson</div><div>J. Danesh</div>
BACKGROUND: There is debate about the value of assessing levels of C-reactive protein (CRP) and other biomarkers of inflammation for the prediction of first cardiovascular events. METHODS: We analyzed data from 52 prospective studies that included 246,669 participants without a history of cardiovascular disease to investigate the value of adding CRP or fibrinogen levels to conventional risk factors for the prediction of cardiovascular risk. We calculated measures of discrimination and reclassification during follow-up and modeled the clinical implications of initiation of statin therapy after the assessment of CRP or fibrinogen. RESULTS: The addition of information on high-density lipoprotein cholesterol to a prognostic model for cardiovascular disease that included age, sex, smoking status, blood pressure, history of diabetes, and total cholesterol level increased the C-index, a measure of risk discrimination, by 0.0050. The further addition to this model of information on CRP or fibrinogen increased the C-index by 0.0039 and 0.0027, respectively (P<0.001), and yielded a net reclassification improvement of 1.52% and 0.83%, respectively, for the predicted 10-year risk categories of "low" (<10%), "intermediate" (10% to <20%), and "high" (≥20%) (P<0.02 for both comparisons). We estimated that among 100,000 adults 40 years of age or older, 15,025 persons would initially be classified as being at intermediate risk for a cardiovascular event if conventional risk factors alone were used to calculate risk. Assuming that statin therapy would be initiated in accordance with Adult Treatment Panel III guidelines (i.e., for persons with a predicted risk of ≥20% and for those with certain other risk factors, such as diabetes, irrespective of their 10-year predicted risk), additional targeted assessment of CRP or fibrinogen levels in the 13,199 remaining participants at intermediate risk could help prevent approximately 30 additional cardiovascular events over the course of 10 years. CONCLUSIONS: In a study of people without known cardiovascular disease, we estimated that under current treatment guidelines, assessment of the CRP or fibrinogen level in people at intermediate risk for a cardiovascular event could help prevent one additional event over a period of 10 years for every 400 to 500 people screened. (Funded by the British Heart Foundation and others.) CopyrightAdult height and the risk of cause-specific death and vascular morbidity in 1 million people: Individual participant meta-analysishttp://repub.eur.nl/pub/67872/
Mon, 01 Oct 2012 00:00:01 GMT<div>D. Wormser</div><div>E. di Angelantonio</div><div>S. Kaptoge</div><div>A.M. Wood</div><div>P. Gao</div><div>Q. Sun</div><div>G. Walldius</div><div>R. Selmer</div><div>W.M. Monique Verschuren</div><div>H.B. Bueno-De-Mesquita</div><div>G. Engström</div><div>P.M. Ridker</div><div>I. Njølstad</div><div>H. Iso</div><div>I. Holme</div><div>S. Giampaoli</div><div>H. Tunstall-Pedoe</div><div>J.M. Gaziano</div><div>E. Brunner</div><div>F. Kee</div><div>A. Tosetto</div><div>C. Meisinger</div><div>H. Brenner</div><div>P. Ducimetiere</div><div>P. Whincup</div><div>A. Tipping</div><div>I. Ford</div><div>P. Cremer</div><div>A. Hofman</div><div>L. Wilhelmsen</div><div>R. Clarke</div><div>I.H. de Boer</div><div>J.W. Jukema</div><div>A.M. Ibañez</div><div>D.A. Lawlor</div><div>R.B. D'Agostino</div><div>B. Rodriguez</div><div>E. Casiglia</div><div>C.D. Stehouwer</div><div>L.A. Simons</div><div>P.J. Nietert</div><div>E. Barrett-Connor</div><div>D.B. Panagiotakos</div><div>C. Björkelund</div><div>T.E. Strandberg</div><div>S. Wassertheil-Smoller</div><div>D.G. Blazer</div><div>T. Meade</div><div>L. Welin</div><div>K. Svärdsudd</div><div>M. Woodward</div><div>A. Nissinen</div><div>D. Kromhout</div><div>T. Jorgensen</div><div>R.S. Tilvis</div><div>J.M. Guralnik</div><div>A. Rosengren</div><div>J. Taylor</div><div>S. Kiechl</div><div>G.R. Dagenais</div><div>F.G.R. Fowkes</div><div>R.B. Wallace</div><div>K-T. Khaw</div><div>J.A. Shaffer</div><div>M. Visser</div><div>J. Kauhanen</div><div>J.T. Salonen</div><div>J. Gallacher</div><div>Y. Ben-Shlomo</div><div>A. Kitamura</div><div>J. Sundstrom</div><div>P. Wennberg</div><div>Y. Kiyohara</div><div>M. Daimon</div><div>A.G. de la Cámara</div><div>J. Cooper</div><div>A. Onat</div><div>M.P. Devereux</div><div>K. Mukamal</div><div>R. Dankner</div><div>M.W. Knuiman</div><div>E. Crespo</div><div>R.T. Gansevoort</div><div>U. Goldbourt</div><div>B.G. Nordestgaard</div><div>J.E. Shaw</div><div>M. Mussolino</div><div>H. Nakagawa</div><div>A.E. Fletcher</div><div>L.H. Kuller</div><div>R.F. Gillum</div><div>V. Gudnason</div><div>G. Assmann</div><div>A. Wald</div><div>P.R. Jousilahti</div><div>P. Greenland</div><div>M. Trevisan</div><div>H. Ulmer</div><div>A.S. Butterworth</div><div>A.R. Folsom</div><div>G. Davey-Smith</div><div>F.B. Hu</div><div>J. Danesh</div><div>L.M. Simpson</div><div>I. Jungner</div><div>E.W. Demerath</div><div>N. Franceschini</div><div>P.L. Lutsey</div><div>C. Pitsavos</div><div>C. Chrysohoou</div><div>C. Stefanadis</div><div>R. Atkins</div><div>P.Z. Zimmet</div><div>E.L.M. Barr</div><div>S.G. Wannamethee</div><div>R. Morris</div><div>J. Willeit</div><div>S. Weger</div><div>F. Oberhollenzer</div><div>S. Ebrahim</div><div>J.W.G. Yarnell</div><div>V. Tikhonoff</div><div>D.K. Shay</div><div>D.B. Garside</div><div>S.E. Sutherland</div><div>D.L. Bachman</div><div>M. Keil</div><div>J.R. Kizer</div><div>B.M. Psaty</div><div>A. Tybjaerg-Hansen</div><div>G.B. Jensen</div><div>P. Schnohr</div><div>D. Palmieri</div><div>S. Panico</div><div>A. Pilotto</div><div>D. Vanuzzo</div><div>J. Simons</div><div>J. McCallum</div><div>Y. Friedlander</div><div>C. Phillips</div><div>F.J. Kohout</div><div>J.C. Cornoni-Huntley</div><div>N.J. Wareham</div><div>B. Schöttker</div><div>H. Müller</div><div>D. Rothenbacher</div><div>J.H. Jansson</div><div>C. Donfrancesco</div><div>E. Vartiainen</div><div>K. Harald</div><div>V. Salomaa</div><div>R.S. Vasan</div><div>C.S. Fox</div><div>M. Pencina</div><div>T. Oizumi</div><div>T. Kayama</div><div>T. Kato</div><div>E.M. Bladbjerg</div><div>L. Møller</div><div>J. Jespersen</div><div>A. Chetrit</div><div>F. Lubin</div><div>H. Eriksson</div><div>G. Lappas</div><div>C. Bengtsson</div><div>L. Lissner</div><div>D. Nagel</div><div>S. Miettinen</div><div>H. Arima</div><div>Y. Doi</div><div>T. Ninomiya</div><div>J.M. Dekker</div><div>M.G.A.A.M. Nijpels</div><div>E. Rimm</div><div>C. Willett</div><div>K. Yamagishi</div><div>H. Noda</div><div>S. Kurl</div><div>T.-P. Tuomainen</div><div>S.W. Poppelaars</div><div>D.J.H. Deeg</div><div>B.L. de Stavola</div><div>B. Hedblad</div><div>P. Nilsson</div><div>A. Blokstra</div><div>S.J. Shea</div><div>B. Thorand</div><div>W. Koenig</div><div>A. Döring</div><div>R. Nitsch</div><div>G. Grandits</div><div>A. Tverdal</div><div>W. Nystad</div><div>J.E. Manson</div><div>S.E. Hankinson</div><div>K.A. Bauer</div><div>K.W. Davidson</div><div>S.A. Kirkland</div><div>D. Shimbo</div><div>S. Sato</div><div>K. Miura</div><div>M. Sakurai</div><div>X. Jouven</div><div>S.J.L. Bakker</div><div>P. van der Harst</div><div>H.L. Hillege</div><div>M.R. Garcia-Palmieri</div><div>P. Amouyel</div><div>D. Arveiler</div><div>J. Ferrieres</div><div>H. Schulte</div><div>A.J. de Craen</div><div>N. Sattar</div><div>D.J. Stott</div><div>B. Cantin</div><div>B. Lamarche</div><div>J.-P. Després</div><div>P. Bergstrom</div><div>R.R. Bettencourt</div><div>D.A. Buisson</div><div>T. Aspelund</div><div>G. Sigurdsson</div><div>B. Thorsson</div><div>M.A. Ikram</div><div>H.W. Tiemeier</div><div>J.C.M. Witteman</div><div>R. Tavendale</div><div>G.D.O. Lowe</div><div>J.-L. Yeh</div><div>T. Ali</div><div>V.D. Calhoun</div><div>G. Can</div><div>K. Nakamura</div><div>Y. Morikawa</div><div>E.B. Mathiesen</div><div>M.-L. Løchen</div><div>T. Wilsgaard</div><div>E. Ingelsson</div><div>K. Michaëlsson</div><div>T. Cederholm</div><div>J.E. Buring</div><div>G. Diem</div><div>H. Concin</div><div>F. Rodeghiero</div><div>M. Marmot</div><div>M. Kivimaki</div><div>M. Robertson</div><div>E.J.M. Feskens</div><div>J.M. Geleijnse</div><div>D. Kromhout</div><div>M. Walker</div><div>S. Watson</div><div>M. Alexander</div><div>O.H. Franco Duran</div><div>R. Gobin</div><div>P. Haycock</div><div>S. Kaptoge</div><div>S.R.K. Seshasai</div><div>S. Lewington</div><div>L. Pennells</div><div>E. Rapsomaniki</div><div>S. Sarwar</div><div>A. Thompson</div><div>S.G. Thompson</div><div>I.R. White</div><div>X. Zhao</div>
Background: The extent to which adult height, a biomarker of the interplay of genetic endowment and early-life experiences, is related to risk of chronic diseases in adulthood is uncertain. Methods: We calculated hazard ratios (HRs) for height, assessed in increments of 6.5 cm, using individual-participant data on 174 374 deaths or major non-fatal vascular outcomes recorded among 1 085 949 people in 121 prospective studies. Results: For people born between 1900 and 1960, mean adult height increased 0.5-1 cm with each successive decade of birth. After adjustment for age, sex, smoking and year of birth, HRs per 6.5 cm greater height were 0.97 (95% confidence interval: 0.96-0.99) for death from any cause, 0.94 (0.93-0.96) for death from vascular causes, 1.04 (1.03-1.06) for death from cancer and 0.92 (0.90-0.94) for death from other causes. Height was negatively associated with death from coronary disease, stroke subtypes, heart failure, stomach and oral cancers, chronic obstructive pulmonary disease, mental disorders, liver disease and external causes. In contrast, height was positively associated with death from ruptured aortic aneurysm, pulmonary embolism, melanoma and cancers of the pancreas, endocrine and nervous systems, ovary, breast, prostate, colorectum, blood and lung. HRs per 6.5 cm greater height ranged from 1.26 (1.12-1.42) for risk of melanoma death to 0.84 (0.80-0.89) for risk of death from chronic obstructive pulmonary disease. HRs were not appreciably altered after further adjustment for adiposity, blood pressure, lipids, inflammation biomarkers, diabetes mellitus, alcohol consumption or socio-economic indicators. Conclusion: Adult height has directionally opposing relationships with risk of death from several different major causes of chronic diseases. Published by Oxford University Press on behalf of the International Epidemiological AssociationMortality from circulatory diseases by specific country of birth across six European countries: Test of concepthttp://repub.eur.nl/pub/56546/
Fri, 01 Jun 2012 00:00:01 GMT<div>R.S. Bhopal</div><div>S.B. Rafnsson</div><div>C.O. Agyemang</div><div>A. Fagot-Campagna</div><div>S. Giampaoli</div><div>N. Hammar</div><div>S. Harding</div><div>K.O. Hedlund</div><div>K. Juel</div><div>J.P. Mackenbach</div><div>P. Primatesta</div><div>G. Rey</div><div>A. Rosato</div><div>S.H. Wild</div><div>A.E. Kunst</div>
Background: Important differences in cardiovascular disease (CVD) mortality by country of birth have been shown within European countries. We now focus on CVD mortality by specific country of birth across European countries. Methods: For Denmark, England and Wales, France, The Netherlands, Scotland and Sweden mortality information on circulatory disease, and the subcategories of ischaemic heart disease, and cerebrovascular disease, was analysed by country of birth. Information on population was obtained from census data or population registers. Directly age-standardized rates per 100000 were estimated by sex for each country of birth group using the WHO World Standard population 2000-25 structure. For differences in the results, at least one of the two 95 confidence intervals did not overlap. Results: Circulatory mortality was similar across countries for men born in India (355.7 in England and Wales, 372.8 in Scotland and 244.5 in Sweden). For other country of birth groups -China, Pakistan, Poland, Turkey and Yugoslavia -there were substantial between-country differences. For example, men born in Poland had a rate of 630.0 in Denmark and 499.3 in England and Wales and 153.5 in France; and men born in Turkey had a rate of 439.4 in Denmark and 231.4 in The Netherlands. A similar pattern was seen in women, e.g. Poland born women had a rate of 264.9 in Denmark, 126.4 in England and Wales and 54.4 in France. The patterns were similar for ischaemic heart disease mortality and cerebrovascular disease mortality. Conclusion: Cross-country comparisons are feasible and the resulting findings are interesting. They merit public health consideration.Cerebral changes on MRI and cognitive function: The CASCADE studyhttp://repub.eur.nl/pub/66700/
Sun, 01 Jan 2006 00:00:01 GMT<div>H. Söderlund</div><div>L.G. Nilsson</div><div>K. Berger</div><div>M.M.B. Breteler</div><div>C. Dufouil</div><div>R. Fuhrer</div><div>S. Giampaoli</div><div>A. Hofman</div><div>A. Pajak</div><div>M.d. Ridder</div><div>S. Sans</div><div>R. Schmidt</div><div>L.J. Launer</div>
The aging, non-demented brain undergoes several physiological changes, some of which may affect cognitive function. The goal of the present study was to examine the associations between subcortical and periventricular white matter hyperintensities (WMHs), cortical and subcortical atrophy, and cognitive function (episodic memory, word fluency, attention, and perceptual, cognitive, and motor speed). This was done within a European collaborative study, Cardiovascular Determinants of Dementia (CASCADE), in which magnetic resonance imaging (MRI) was performed on community-dwelling individuals. The study includes 1254 persons from eight European study centers, ranging between 64 and 76 years of age (M 69.4 ± 3.3; 55% men). When demographics (age, education, and sex), study center, and concurrent brain changes had been adjusted for, periventricular WMHS predicted lower performance in word fluency and the Stroop test (time), and subcortical atrophy predicted lower performance in motor speed and the Stroop test (errors). The findings are consistent with findings from lesion and functional neuroimaging studies.Regional variability in the prevalence of cerebral white matter lesions: An MRI study in 9 European countries (CASCADE)http://repub.eur.nl/pub/63660/
Thu, 01 Dec 2005 00:00:01 GMT<div>L.J. Launer</div><div>K. Berger</div><div>M.M.B. Breteler</div><div>C. Dufouil</div><div>R. Fuhrer</div><div>S. Giampaoli</div><div>L.G. Nilsson</div><div>A. Pajak</div><div>M.A.J. de Ridder</div><div>E.J. van Dijk</div><div>S. Sans</div><div>R. Schmidt</div><div>A. Hofman</div>
White matter lesions (WML) on MRI of the brain are common in both demented and nondemented older persons. They may be due to ischemic events and are associated with cognitive and physical impairments. It is not known whether the prevalence of these WML in the general population differs across European countries in a pattern similar to that seen for coronary heart disease. Here we report the prevalence of WML in 1,805 men and women drawn from population-based samples of 65- to 75-year-olds in ten European cohorts. Data were collected using standardized methods as a part of the multicenter study CASCADE (Cardiovascular Determinants of Dementia). Centers were grouped by region: south (Italy, Spain, France), north (Netherlands, UK, Sweden), and central (Austria, Germany, Poland). In this 10-year age stratum, 92% of the sample had some lesions, and the prevalence increased with age. The prevalence of WML was highest in the southern region, even after adjusting for differences in demographic and selected cardiovascular risk factors. Brain aging leading to disabilities will increase in the future. As a means of hypothesis generation and for health planning, further research on the geographic distribution of WML may lead to the identification of new risk factors for these lesions. CopyrightCognitive test battery of CASCADE: Tasks and datahttp://repub.eur.nl/pub/59628/
Tue, 01 Mar 2005 00:00:01 GMT<div>L.G. Nilsson</div><div>H. Söderlund</div><div>K. Berger</div><div>M.M.B. Breteler</div><div>M.A.J. de Ridder</div><div>C. Dufouil</div><div>R. Fuhrer</div><div>S. Giampaoli</div><div>A. Hofman</div><div>A. Pajak</div><div>S. Sans</div><div>R. Schmidt</div><div>L.J. Launer</div>
This paper presents the cognitive test battery used in the CASCADE Study (Cardiovascular Determinants of Dementia) for examining the consequences of cerebral white matter lesions and atrophy. The test battery includes nine different tasks assessing memory, executive function, and global cognitive function. Three episodic memory tasks were used in combinations to assess the role of attention and speed on encoding. Estimates of short- and long-term memory capacity were also derived from these three memory tasks. Semantic memory production/frontal lobe functions were assessed by means of a word fluency test. The Letter Digit Substitution test and the Stroop test were used to assess speed of processing and attention. Motor speed was measured with the Purdue Pegboard test, and global cognitive function was assessed by the Mini Mental State Examination. Overall performance data for the whole CASCADE sample and for each of eight study centers are presented for each test. Possible reasons for performance differences among study centers are discussed. CopyrightThe association between blood pressure, hypertension, and cerebral white matter lesions: cardiovascular determinants of dementia study.http://repub.eur.nl/pub/13510/
Mon, 01 Nov 2004 00:00:01 GMT<div>E.J. van Dijk</div><div>M.M.B. Breteler</div><div>R. Schmidt</div><div>K. Berger</div><div>L.G. Nilsson</div><div>M. Oudkerk</div><div>A. Pajak</div><div>S. Sans</div><div>M.A.J. de Ridder</div><div>C. Dufouil</div><div>R. Fuhrer</div><div>S. Giampaoli</div><div>L.J. Launer</div><div>A. Hofman</div>
Cerebral white matter lesions are frequently observed on magnetic
resonance imaging (MRI) scans in elderly people and are associated with
stroke and dementia. Elevated blood pressure is presumed one of the main
risk factors, although data are almost exclusively derived from
cross-sectional studies. We assessed in 10 European cohorts the relation
between concurrently and previously measured blood pressure levels,
hypertension, its treatment, and severe cerebral white matter lesions. In
total, 1805 nondemented subjects aged 65 to 75 years were sampled from
ongoing community-based studies that were initiated 5 to 20 years before
the MRI. White matter lesions in the periventricular and subcortical
region were rated separately using semiquantitative measures. We performed
logistic regression analyses adjusted for potential confounders in 1625
people with complete data. Concurrently and formerly assessed diastolic
and systolic blood pressure levels were positively associated with severe
white matter lesions. Both increases and decreases in diastolic blood
pressure were associated with more severe periventricular white matter
lesions. Increase in systolic blood pressure levels was associated with
more severe periventricular and subcortical white matter lesions. People
with poorly controlled hypertension had a higher risk of severe white
matter lesions than those without hypertension, or those with controlled
or untreated hypertension. Higher blood pressure was associated with an
increased risk of severe white matter lesions. Successful treatment of
hypertension may reduce this risk; however, a potential negative effect of
decreasing diastolic blood pressure level on the occurrence of severe
periventricular white matter lesions should be taken into account.Magnetic Resonance Imaging of the Brain in Diabetes: The Cardiovascular Determinants of Dementia (CASCADE) Studyhttp://repub.eur.nl/pub/54925/
Mon, 01 Mar 2004 00:00:01 GMT<div>R. Schmidt</div><div>L.J. Launer</div><div>L.G. Nilsson</div><div>A. Pajak</div><div>S. Sans</div><div>K. Berger</div><div>M.M.B. Breteler</div><div>M.A.J. de Ridder</div><div>C. Dufouil</div><div>R. Fuhrer</div><div>S. Giampaoli</div><div>A. Hofman</div>